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Ovum Transport

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Infusions of VIP for 60 min at the P peak, and for 240 min at the time of ovulation, had no significant effect upon ovum pickup or the rate of ovum transport[9].

Administration of progesterone (im, 2.5 mg) produced complete relaxation of both isthmus and ampulla, did not produce increased isthmic contractility on coitus, accelerated the ovum transport rate and inhibited pregnancy, again emphasising the ova retentive role of oviductal motility [10].

We suggest that a rise in pelvic venous pressure could lead to a decrease in isthmic luminal diameter and thus act as a sphincter contributing to the known delay in ovum transport at the ampullary isthmic junction [11].

The results described are consistent with the hypothesis that differential sperm and ovum transport in the human fallopian tube isthmus is at least partially determined by the presence or absence of estrogen-dependent luminal mucus [12].

Our data suggest that normal tubal patency and ovum transport function can be tested by introducing radioactive ovum surrogates of appropriate size into the oviducts and monitoring their time of arrival at the uterus[13].

Thus, RU486 failed to accelerate ovum transport during the first three days of treatment in pregnant rats, in spite of the fact that no progesterone receptors were available in the oviduct as early as 24 h of treatment [8].

To test the hypothesis that a primary (although undefined) disturbance of ovum transport may lead to faulty uterine implantation and so to abortion, the author examined the case records of 273 patients who underwent nonmicrosurgical bilateral tubal surgery for infertility at King George V Memorial Hospital, Sydney, between 1966 and 1975 [18].